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Biomedical subjects

A M Bronstein

Publications and source records attributed to A M Bronstein.

At least 73 records · Page 4Linked to original sources
PubMed1998

Upbeat nystagmus: clinicoanatomical correlation.

A patient is reported on with isolated upbeating nystagmus with a linear slow phase in whom a solitary lesion, probably inflammatory, was detected radiologically in the dorsal paramedian caudal medulla, encompassing the most caudal of the perihypoglossal nuclei, the nucleus intercalatus of Staderini. The conjunction of a vestibular pattern of nystagmus with this focal lesion runs contrary to a previous suggestion that the nucleus intercalatus may act as a neural integrator for vertical conjugate eye movements.

Adult↗
PubMed1998

Vestibular hypersensitivity to clicks is characteristic of the Tullio phenomenon.

OBJECTIVES: The frequency of pathologically reduced click thresholds for vestibular activation was explored in patients with the Tullio phenomenon (sound induced vestibular activation). METHODS: Seven patients (eight affected ears) with symptoms of oscillopsia and unsteadiness in response to loud external sounds or to the patient's own voice were examined. In all but one patient, vestibular hypersensitivity to sound was confirmed by the fact that eye movements could be produced by pure tones of 110 dB intensity or less. Conventional diagnostic imaging was normal in all cases and three of the patients had normal middle ears at surgical exploration. Thresholds for click evoked vestibulocollic reflexes were compared with those of a group of normal subjects. Galvanic stimulation was used as a complementary method of examining the excitability of vestibular reflexes. RESULTS: All the patients showed a reduced threshold for click activation of vestibulocollic reflexes arising from the affected ear. Short latency EMG responses to clicks were also present in posterior neck and leg muscles, suggesting that these muscles receive vestibular projections. Galvanic stimulation produced a normal pattern of body sway in four of the five patients tested. CONCLUSIONS: A pathologically reduced threshold to click activation (< or = 70 dB NHL (average normal hearing level)) seems to be a consistent feature of the Tullio phenomenon and a useful diagnostic criterion. This in turn is most likely to be due to an increased effectiveness of the transmission of sound energy to saccular receptors. Activation of these receptors probably contributed to the vestibular symptoms experienced by the patients.

Acoustic Stimulation↗
PubMed1998

Oscillopsia: visual function during motion in the absence of vestibulo-ocular reflex.

OBJECTIVES: To investigate (1) the effects of loss of vestibular function on spatiotemporal vision and (2) the mechanisms which enable labyrinthine defective (LD) patients to adapt to oscillopsia. METHODS: Visual function and eye movements were assessed in seven normal subjects and four LD patients with oscillopsia due to absent vestibulo-ocular reflex. Temporal vision was assessed by measurement of threshold sensitivity for detection of a target which moved across a flickering, spatially uniform background field. Spatial vision was investigated by measurements of threshold sensitivity for the detection of a target moving across a spatially modulated background in the form of square wave gratings. Velocity discrimination was assessed with drifting gratings. All measurements were made under static conditions and during oscillatory movement of either the visual stimulus or the subject (1 Hz, peak velocity 50 degrees/s). RESULTS: Temporal responses--Normal subjects and LD patients exhibited similar responses while static and under body oscillation. Spatial responses--The two groups achieved similar results under static conditions but body oscillation reduced threshold sensitivities and shifted the spatial response function towards lower spatial frequencies in the LD patients only. Similar changes in the spatial responses were seen during oscillation of the visual stimulus but these occurred in both normal subjects and LD patients. Velocity discrimination--Two LD patients achieved normal velocity discrimination but the other two showed abnormal responses to visual stimulus movement; one displayed a loss of velocity discrimination during whole body oscillation, and the other mismatched the velocity of two moving grating stimuli. CONCLUSIONS: The changes in the spatial responses are attributed to the presence of retinal slip during visual stimulus motion in all subjects or body oscillation in the LD patients. It is concluded that any visual adaptation to oscillopsia achieved by the LD patients does not influence the measured spatial response functions, which arise at an early stage of visual processing. The abnormal velocity discrimination may relate to the progressive improvement in oscillopsia reported by LD patients.

Adult↗
PubMed1997

Selective vestibular damage in neurosarcoidosis.

We report a patient with neurosarcoidosis who developed bilateral benign paroxysmal positional vertigo (BPPV) of the posterior canals, deafness, and absent responses to conventional caloric and rotational vestibular testing. Additional rotation in the planes of the vertical semicircular canals revealed relative sparing of vertical canal function. This vertical-horizontal canal dissociation explains the presence of BPPV and suggests that the vestibular damage in this patient is secondary to a vasculitic neuropathy.

Adult↗
PubMed1997

Torticollis due to disinhibition of the vestibulo-collic reflex in a patient with Steele-Richardson-Olszewski syndrome.

A patient with the clinical picture of Steele-Richardson-Olszewski syndrome and an unusual intermittent neck twisting is reported. He had virtually no voluntary ocular movements and only very slow, low-amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained deviated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo-collic reflex and a disturbed head position resetting mechanism. Neck electromyographic responses in response to whole-body rotation indicated that the vestibulocollic reflex responsible for the torticollis in this patient had a short latency of approximately 30 ms.

Amygdala↗
PubMed1997

Perception of spatial orientation in spasmodic torticollis. Part I: The postural vertical.

Estimates of points of entering and exiting from upright posture were obtained from 25 seated, restrained patients with idiopathic spasmodic torticollis (ST) and matched normal subjects exposed to cycles of 1.5 degrees/s tilts in a flight simulator. Estimates were obtained for displacements in roll and pitch about upright and for yaw tilts about a rostrocaudal, "barbecue," axis with the subjects supinated. For both pitch and roll, normal subjects estimated entering upright when they were still approximately 1 degree from machine upright and perceived themselves to be upright through a mean arc of 6 degrees. In barbecue tilt, entering upright was estimated at 0.2 degree for an arc of 6 degrees. Patients estimated entering upright at 2.8 degrees in roll and 3 degrees in pitch but estimated exiting upright at the same tilt as normal subjects; that is, they were less specific in detecting verticality. Patients were normal in barbecue tilt. No relationship between tilt estimates and head deviation was found. There were no differences between normal subjects when tested with their head in normal posture and with an assumed tilt of 20 degrees. Normal subjects probably based their estimates on combined vestibular-somatosensory signals, whereas torticollis patients appeared to derive more from a vestibular signal. However, patients referred the vestibular signals to the trunk long axis when asked to indicate the whole-body vertical. The findings suggest disruption of the normal combined vestibuloproprioceptive mechanism for detecting body uprightness in ST.

Adult↗
PubMed1997

Perception of spatial orientation in spasmodic torticollis. Part 2: The visual vertical.

Twenty-nine patients with idiopathic spasmodic torticollis (ST) and matched normal control subjects were asked to align a target line to perceived earth vertical [visual vertical (VV)]. Settings were made against a whole-field random-dot background that was either stationary or rotating around the line of sight, and subjects performed the task upright and lying horizontally on their sides. Normal subjects were tested both head upright and after assuming a voluntary head tilt. Patients with ST set the VV close to true upright with a minimal deviation toward tilt of the head in contrast to normal subjects assuming a head tilt who set the VV in the opposite direction to the head tilt (Müller "E" effect). Settings against the spinning disk were biased in the direction of rotation similarly for both subject groups. Settings made against static or spinning disk performed when subjects lay horizontally were tilted in the direction of recumbence (Aubert "A" effect) similarly for both subject groups. When attempting to set the target line parallel to the long axis of the face, patients with head tilt set the line to upright, whereas normal subjects correctly estimated their tilts. One hypothesis offered to explain these results is that the patients referenced only their upright trunk for vertical and did not make use of neck proprioceptive or vestibular signals of head tilt so that all settings were made as if the trunk and head were upright. Alternatively, patients may have used only otolith signals as the reference for upright, and these are recalibrated in ST patients with head tilt. The pathological deviation becomes accepted as upright posture, and VVs and facial orientation are estimated as if the head were upright. In either case the findings indicate abnormal processing of the perception of visual verticality in ST patients.

Adult↗
PubMed1997

Automatic control of postural sway by visual motion parallax.

The purpose of this study was to establish whether visual motion parallax participates in the control of postural sway. Body sway was measured in ten normal subjects by photoelectric recordings of head movements and by force-plate posturography. Subjects viewed a visual display ("background"), which briefly moved (2 s) along the y (horizontal) axis, under three different conditions: (1) direct fixation of the background, (2) fixation of a stationary window frame in the foreground, and (3) fixation of the background in the presence of the window in the foreground ("through the window"). In response to background fixation, subjects swayed in the same direction as stimulus motion, but during foreground (window) fixation they swayed in the opposite direction. The earlier forces observed on the force platform occurred at circa 250 ms in both conditions. The results show that motion parallax generates postural responses. The direction of these parallax-evoked postural responses-opposite to other visually evoked postural responses reported so far-is appropriate for stabilizating posture in natural circumstances. The findings show that motion parallax is an important source of self-motion information and that this information participates in the process of automatic postural control. In the "fixating through the window" condition, which does not mimic visual conditions induced by body sway, no consistent postural responses were elicited. This implies that postural reactions elicited by visual motion are not rigid responses to optokinetic stimulation but responses to visual stimuli signalling self-motion.

Adult↗
PubMed1997

Eye movements induced by lateral acceleration steps. Effect of visual context and acceleration levels.

Eye movement responses were obtained from six normal subjects exposed to randomly ordered rightwards/leftwards linear acceleration steps of 0.05 g, 0.1 g or 0.24 g amplitude and 650 ms duration along the interaural axis. With the instruction to gaze passively into the darkness, compensatory nystagmus was evoked with slow-phase velocity sensitivity of 49 degrees s(-1) g(-1). When subjects viewed earth-fixed targets at 30 cm, 60 cm or 280 cm, eye movements at 130 ms from motion onset were proportional to acceleration and inversely proportional to target distance, before the onset of visually guided eye movements. Our results show that a modulation with viewing distances of the earliest human otolith-ocular reflexes occurs in the presence of pure linear acceleration. However, full compensation was not attained for the nearer targets and higher accelerations.

Acceleration↗
PubMed1997

Hyperventilation effect on postural sway.

OBJECTIVE: To examine the effect of voluntary hyperventilation (HV) on postural sway. DESIGN: Crossover controlled, experimental study. SETTING: Human movement and balance clinical research unit. SUBJECTS: Four different groups of normal subjects (n = 6, 6, 7, and 9) and patients with bilateral absence of vestibular function (n = 9). INTERVENTION: Partial carbon dioxide pressure (tc-PCO2) was measured transcutaneously with surface electrodes. Body sway was measured with a force platform immediately after maximal voluntary HV for 30 to 90 seconds. Recordings were obtained with eyes open and eyes closed, standing on the platform and on foam-rubber, and after head or body movements. MAIN OUTCOME MEASURE: Postural sway. RESULTS: HV increased body sway in all conditions, but the effects were more intense when subjects were standing directly on the platform surface with their eyes closed. Recordings after HV of 30, 60, and 90 sec in normal subjects showed that although CO2 levels were inversely related to the duration of HV, body sway did not increase further. HV also increased sway after active movements by the subjects. The main sway increase was in sway area and mean and maximal deviations but less for mean sway velocity. HV preferentially increased low-frequency sway oscillations. These effects were also present in labyrinthine-defective subjects. CONCLUSIONS: HV increases body sway, but the relationship between CO2 levels and degree of unsteadiness is not linear. The dizziness reported by patients with HV syndrome may be partly caused by objective unsteadiness. The presence of HV-induced unsteadiness in patients with absent vestibular function indicates that the effects of HV are not mediated by the labyrinth.

Adult↗
PubMed1997

Effect of otolith dysfunction. Impairment of visual acuity during linear head motion in labyrinthine defective subjects.

Visual symptoms emerging after the loss of vestibular function are usually attributed to the dysfunction of semicircular canal vestibulo-ocular reflexes, as they have been shown to stabilize vision during angular head movements. However, natural head displacements involve both angular and linear motion, and therefore visual instability may occur because of defective otolith-ocular reflexes (OORs) which are the eye movements evoked by linear head acceleration. In this paper, the relationship between OORs and visual acuity during linear head motion was studied in normal subjects and 14 patients with bilateral loss of caloric responses. OORs were elicited in darkness by step acceleration (0.24 g) of the whole body along the interaural axis. Latency, slow phase velocity and asymmetry of the OOR were measured from the desaccaded and averaged electrooculographic trace. Visual acuity was assessed during sinusoidal lateral oscillation of the subject viewing an earth-fixed target, and vice versa with the subject stationary and the target moving at 0.5, 1.0 and 1.5 Hz. The task was to recognize numbers flashing up on a three digit light-emitting diode visual display. Normal subjects had symmetrical OORs with short latencies (< 130 ms). In patients, OORs were either absent (n = 2) or abnormal with asymmetries (n = 8), diminished velocities (n = 4) or prolonged latencies (n = 6). At high frequency oscillation (1.5 Hz), normal subjects invariably recognized more numbers during self-motion compared with target motion, whereas most patients did not. In patients, abnormal dynamic visual acuity was correlated with absent or delayed OOR responses. This is the first demonstration of a functional role of the OORs in that they contribute to visual stabilization during high frequency linear head motion. Bilateral vestibular failure commonly affects the OORs and thereby compromises dynamic visual acuity.

Acceleration↗
PubMed1997

The effects of hyperventilation on postural control mechanisms.

The effect of hyperventilation on postural balance was investigated. Voluntary hyperventilation increased body sway in normal subjects, particularly in the sagittal plane. The possibility that this hyperventilation-induced unsteadiness is due to interference with lower limb somatosensory input, vestibular reflexes or cerebellar function was assessed. (i) The effect of hyperventilation on peripheral compound sensory action potentials (SAPs) and somatosensory evoked potentials (SEPs) (recorded centrally, from the scalp) elicited by electrical stimulation of the sural nerve was measured in six normal adults. A reduction in the scalp SEP amplitude and an increase in the peripheral SAP amplitude were observed during hyperventilation, which reversed during the recovery period. These changes indicate increased peripheral neural excitability which could lead to a higher level of ectopic activity; the latter would interfere with central reception of peripheral input. (ii) The click-evoked vestibulo-collic reflex was recorded to study the effect of hyperventilation on vestibulo-spinal activity. EMG recordings from both sternocleidomastoid muscles of six healthy subjects were made in response to loud clicks presented to either ear. Neither the amplitude nor the latency of the response were altered significantly by hyperventilation. (iii) Eye-movement recordings were obtained in the six normal subjects to assess the effect of hyperventilation on the vestibulo-ocular reflex and its visual suppression, the latter being a function largely mediated by the cerebellum; no changes were detected. (iv) Three-dimensional eye-movement recordings and body-sway measurements were obtained in six patients with longstanding unilateral vestibular loss in order to evaluate if hyperventilation disrupts vestibular compensation. In all patients, a horizontal nystagmus either appeared or was significantly enhanced for > or = 60 s after voluntary hyperventilation. Sway was also enhanced by hyperventilation in these patients, particularly in the frontal plane. This study suggests that hyperventilation disrupts mechanisms mediating vestibular compensation. The increase in sway may be, at least partly, mediated by deranged peripheral and central somatosensory signals from the lower limbs. Hyperventilation seems to spare vestibular reflex activity and cerebellar-mediated eye movements.

Acoustic Stimulation↗
PubMed1997

Three hundred sixty-degree rotation of the posterior semicircular canal for treatment of benign positional vertigo: a placebo-controlled trial.

The canalithiasis hypothesis proposes that benign positional vertigo (BPV) is caused by dislodged otoconia that settle in the posterior semicircular canal (PSC). When head position is changed these particles move within the canal and induce abnormal endolymph flow. To clear the PSC from debris we developed a procedure that consists of a full circle of backward head rotation in the exact plane of the canal. Patients were seated in a three-dimensional motion device that rotated in steps of 110 degrees every 30 seconds. The first part of the study was conducted as an open trial; the second part followed a single-blinded, placebo-controlled design: Forward rotation (placebo) was applied first and backward rotation was applied 1 week later if BPV persisted. All patients were assessed with a symptom diary and, in the controlled trial, also with the Dix-Hallpike maneuver. In the open study 10 of 15 patients became asymptomatic after one treatment session. In the controlled trial all 15 patients remained symptomatic after forward rotation while 10 of 14 undergoing backward rotation were relieved from positional vertigo immediately (p = 0.004). The presence of secondary nystagmus during the procedure indicated a favorable outcome. Our findings provide evidence for the efficacy of canal-clearing procedures that validate the canalithiasis hypothesis of BPV.

Calculi↗
PubMed1997

Horizontal otolith-ocular responses to lateral translation in benign paroxysmal positional vertigo.

Benign paroxysmal positional vertigo (BPPV) is assumed to result from utricular damage, but it is controversial if patients have manifest utricular dysfunction. Therefore, we investigated linear vestibulo-ocular reflexes (LVORs) during lateral whole-body translation in 14 patients with unilateral BPPV. Patients were subjected to linear acceleration steps of 0.24 g along the interaural axis, which were applied randomly to the left and right, both in the dark and in the light with a visual target at a distance of 60 cm. The LVOR was measured by EOG from the slow phase velocity of the averaged and desaccaded compensatory eye movement. In normal cases, maximum asymmetry of LVOR velocity was 13% in the dark and 10% in the light. In patients, LVOR velocities were normal in the dark but mildly reduced in the light (p < 0.05). Five patients had mild LVOR asymmetries in the dark (range 18-38%) and two in the light (11 and 13%), but there was no consistent relationship to the affected side. The absence of gross changes of the LVOR may be explained either by minor utricular damage that is functionally irrelevant or by central compensation of a chronic unilateral deficit.

Adult↗
PubMed1996

Reflex (unloading) and (defensive capitulation) responses in human neck muscle.

1. We studied unloading and stretch responses in human neck muscle during manoeuvres in which the head pulled against a 2-3 kg weight which could be abruptly released or applied electromagnetically. 2. During head tracking in pitch, unloading of the weight induced inhibition of EMG in the contracting sternocleidomastoid at a mean latency of 24.9 ms in normal subjects and at 41 ms in bilateral labyrinthine-defective subjects, with antagonist (trapezius) excitation at 30.5 and 41.3 ms, respectively. During tracking in yaw, unloading induced inhibition in the contracting splenius capitis (SpC) at a mean latency of 20.4 ms in normal subjects and 25 ms in labyrinthine-defective subjects, with excitation in the antagonist SpC at 22.2 and 24 ms, respectively. 3. If subjects tried to resist an unexpected sideways tug on the head a burst occurred in the stretched SpC at a mean latency of 53.5 ms. When subjects relaxed there was excitation of the shortening of SpC at 75.9 ms, which assisted the imposed motion and is possibly a "defensive reflex".

Adult↗